Cross-sectional and a few longitudinal studies in both humans and other primates have determined that a limited number of subgingival bacteria are potential periodontopathogens and may be associated with disease initiation and/or progression. Our progress during this past grant period has been: 1) clear demonstration of the microbiological, immunological, and clinical similarities between our Nhp model of ligature-induced periodontitis and adult periodontitis in humans; 2) the development of techniques for objectively quantitating the initiation of periodontitis; 3) the demonstration that at lease two clinical and microbiological forms of periodontitis exist in the Nhp model; a slowly progressing form, as well as a disease characterized by "bursts" of activity; and 4) that a single periodontopathogen, when implanted into the complex ecosystem of the Nhp periodontium, may produce these bursts of disease activity. We will use the techniques and experimental approaches employed in the last grant period to extend previous associational observations and to focus our efforts to determine: 1) the exact characteristics of disease initiation and progression in animals which exhibit slowly progressing and bursts of disease; 2) the impact of implanting specific periodontopathic microorganisms into the subgingival microbiota and the impact of these putative pathogens on disease initiation; 3) how the specific antibody response to these microorganisms correlates with the kinetics of disease progression; and 4) the role of the specific antibody response in regulating bacterial colonization and emergence in the subgingival microbiota. In general, these proposed studies represent what may be one of the first longitudinal evaluations of the initiation of periodontitis and are designed to determine the temporal relationship(s) between the acquisition of specific putative periodontopathogens, the specific antibody response, and disease initiation.